Search

Your search keyword '"Arcos-Fajardo, Michelle"' showing total 6 results
Start Over Author "Arcos-Fajardo, Michelle" Publisher rockefeller university press
6 results on '"Arcos-Fajardo, Michelle"'

1. Transglutaminase is essential for IgA nephropathy development acting through IgA receptors

Author

Berthelot, Laureline, primary, Papista, Christina, additional, Maciel, Thiago T., additional, Biarnes-Pelicot, Martine, additional, Tissandie, Emilie, additional, Wang, Pamela H.M., additional, Tamouza, Houda, additional, Jamin, Agnès, additional, Bex-Coudrat, Julie, additional, Gestin, Aurelie, additional, Boumediene, Ahmed, additional, Arcos-Fajardo, Michelle, additional, England, Patrick, additional, Pillebout, Evangéline, additional, Walker, Francine, additional, Daugas, Eric, additional, Vrtosvnik, François, additional, Flamant, Martin, additional, Benhamou, Marc, additional, Cogné, Michel, additional, Moura, Ivan C., additional, and Monteiro, Renato C., additional

Published
2012
Full Text
View/download PDF

2. Secretory IgA mediates retrotranscytosis of intact gliadin peptides via the transferrin receptor in celiac disease

Author

Matysiak-Budnik, Tamara, primary, Moura, Ivan Cruz, additional, Arcos-Fajardo, Michelle, additional, Lebreton, Corinne, additional, Ménard, Sandrine, additional, Candalh, Céline, additional, Ben-Khalifa, Karima, additional, Dugave, Christophe, additional, Tamouza, Houda, additional, van Niel, Guillaume, additional, Bouhnik, Yoram, additional, Lamarque, Dominique, additional, Chaussade, Stanislas, additional, Malamut, Georgia, additional, Cellier, Christophe, additional, Cerf-Bensussan, Nadine, additional, Monteiro, Renato C., additional, and Heyman, Martine, additional

Published
2008
Full Text
View/download PDF

3. Secretory IgA mediates retrotranscytosis of intact gliadin peptides via the transferrin receptor in celiac disease

Author

Matysiak-Budnik, Tamara, primary, Moura, Ivan Cruz, additional, Arcos-Fajardo, Michelle, additional, Lebreton, Corinne, additional, Ménard, Sandrine, additional, Candalh, Céline, additional, Ben-Khalifa, Karima, additional, Dugave, Christophe, additional, Tamouza, Houda, additional, van Niel, Guillaume, additional, Bouhnik, Yoram, additional, Lamarque, Dominique, additional, Chaussade, Stanislas, additional, Malamut, Georgia, additional, Cellier, Christophe, additional, Cerf-Bensussan, Nadine, additional, Monteiro, Renato C., additional, and Heyman, Martine, additional

Published
2007
Full Text
View/download PDF

6. Secretory IgA mediates retrotranscytosis of intact gliadin peptides via the transferrin receptor in celiac disease.

Author

Matysiak-Budnik T, Moura IC, Arcos-Fajardo M, Lebreton C, Ménard S, Candalh C, Ben-Khalifa K, Dugave C, Tamouza H, van Niel G, Bouhnik Y, Lamarque D, Chaussade S, Malamut G, Cellier C, Cerf-Bensussan N, Monteiro RC, and Heyman M

Subjects
Antigens, CD biosynthesis, Biopsy, Chromatography, High Pressure Liquid, Enterocytes metabolism, Glomerulonephritis, IGA diagnosis, Glomerulonephritis, IGA pathology, Humans, Immunoglobulin A chemistry, Immunohistochemistry methods, Models, Biological, Molecular Weight, Receptors, Transferrin biosynthesis, Celiac Disease metabolism, Gliadin chemistry, Immunoglobulin A metabolism, Peptides chemistry, Receptors, Transferrin chemistry
Abstract

Celiac disease (CD) is an enteropathy resulting from an abnormal immune response to gluten-derived peptides in genetically susceptible individuals. This immune response is initiated by intestinal transport of intact peptide 31-49 (p31-49) and 33-mer gliadin peptides through an unknown mechanism. We show that the transferrin receptor CD71 is responsible for apical to basal retrotranscytosis of gliadin peptides, a process during which p31-49 and 33-mer peptides are protected from degradation. In patients with active CD, CD71 is overexpressed in the intestinal epithelium and colocalizes with immunoglobulin (Ig) A. Intestinal transport of intact p31-49 and 33-mer peptides was blocked by polymeric and secretory IgA (SIgA) and by soluble CD71 receptors, pointing to a role of SIgA-gliadin complexes in this abnormal intestinal transport. This retrotranscytosis of SIgA-gliadin complexes may promote the entry of harmful gliadin peptides into the intestinal mucosa, thereby triggering an immune response and perpetuating intestinal inflammation. Our findings strongly implicate CD71 in the pathogenesis of CD.

Published
2008
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results